We show that nitrated-polycyclic aromatic hydrocarbons (nitro-PAHs) induce cell death in Hepa1c1c7 cells, as measured by fluorescence microscopy. BEAS-2B cells, however did not show any relevant effects. 1.3-DNP induce formation of the active form of both caspase 3 and its intracellular substrate, poly(ADP-ribose)polymerase (PARP). The most important finding was that the most mutagenic and carcinogenic compound, 1.8-DNP, induced a delayed cell death, when compared to 1.3-DNP, despite that this compound seemed to give the same amount of oxidative damage, judged by comet assay, increased phosohorylation of p53 and accumulation of cells in S-phase. 1-NP and 1.3-DNP gave an accumulation of cells in G2-phase. 1.3-DNP seemed to demand a smaller p53 response in order to trigger apoptosis. Immunocytochemical studies revealed that the p53 did accumulate in the nucleus. In addition, we saw some DNA damage response. 1.8-DNP did induce activation of p53 and Chk1, however, no effect was seen on NOXA. These findings suggest that other parallel cell death pathways may be lacking.